Systemic pattern of free radical generation during coronary bypass surgery.

Davies, Simon; Underwood, S.M.; Wickens, D. G.; Feneck, R. O.; Dormandy, T. L.; Walesby, R.K.

doi:10.1136/hrt.64.4.236

Cited by 57 publications

(22 citation statements)

References 36 publications

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“…Myocardial reperfusion during cardiovascular surgery has been shown to increase systemic indices of free radical activity including liberation of lipid peroxides [14,15]. The exact source of free radicals resulting in lipid peroxidation after cardiac surgery is not clear, because some studies found increased lipid peroxides in arterial Inselmann/Köhler/Lange/Silber/Nellessen and mixed venous blood but not in the coronary sinus [14,16]. In contrast, Lazzarino et al [17] found that lipid peroxides increased in the coronary sinus during heart surgery.…”

Section: Discussionmentioning

confidence: 99%

“…Amounts of TBARS were expressed in equivalents of MDA from a standard curve prepared with tetramethoxypropane [13]. In order to adjust for perioperative hemodilution MDA was expressed as nmol/g of albumin [14]. For reference values sera of 9 patients undergoing sterniotomy and following lung operations were analyzed in the same way.…”

Section: Analytical Proceduresmentioning

confidence: 99%

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Lipid Peroxidation and Cardiac Troponin T Release during Routine Cardiac Surgery

et al. 1998

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Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation. The purpose of this study was to monitor perioperative changes of cardiac troponin t and malondialdehyde as an indicator of lipid peroxidation in patients who underwent routine cardiac operation and had no signs of perioperative myocardial infarction. Patients with thoracic surgery alone served as controls. We studied 20 patients with cardiopulmonary bypass (CPB) and 9 patients with other thoracic operations. Serum troponin t, malondialdehyde, myoglobin, creatine kinase (CK) including CK-MB isoenzyme levels were monitored before CPB, immediately after cessation of CPB, 20 and 44 h after CPB. Patients with signs of myocardial infarction before or up to 44 h after surgery were excluded. Of 20 patients with CBP, 18 patients showed a significant increase of troponin t and 16 patients had elevated malondialdehyde serum levels following CPB. Troponin t serum values were raised immediately after CPB to 0.60 ± 0.12 µg/l and increased further to 0.90 ± 0.17 µg/l after 44 h (p < 0.005, in comparison to preoperative: 0.08 ± 0.02 µg/l). Patients undergoing the other thoracic operations showed neither any detectable troponin t serum values nor significant changes of serum malondialdehyde during the observed period. In the CPB group serum malondialdehyde peaked immediately after CPB to 98 ± 9 nmol/g albumin (p < 0.005) and returned to preoperative levels (63 ± 3 nmol/g albumin) within 20 h (60 ± 3 nmol/g albumin). Individual maximal troponin t serum levels did not correlate with individual maximal serum malondialdehyde levels. The observed increase of troponin t levels had no influence on patients’ outcome followed up for 18 months. The results demonstrate that troponin t and lipid peroxidation increase during uncomplicated cardiac surgery in patients without signs of myocardial infarction. Following uncomplicated cardiac surgery, a moderate increase of cardiac troponin t may not reflect severe cardiac injury.

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Section: Discussionmentioning

confidence: 99%

Section: Analytical Proceduresmentioning

confidence: 99%

Lipid Peroxidation and Cardiac Troponin T Release during Routine Cardiac Surgery

et al. 1998

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“…A major contribution to pulmonary injury after CPB is attributed to free oxygen radicals arising from ischemia and reperfusion. 12,13 The rise of free radical levels is more intense in the early reperfusion period. After reperfusion, contact of the ischemic tissue with the molecular oxygen results in the formation of free oxygen radicals in a high proportion, and the longer the ischemic period lasts, the more the free radicals are produced.…”

Section: Discussionmentioning

confidence: 99%

The Efficacy of Vitamin E in the Prevention of Lung Ischemia-Reperfusion Injury After Cardiopulmonary Bypass in Open Heart Surgery

Acipayam¹,

Sunar²,

Canbaz³

et al. 2013

Turkiye Klinikleri J Med Sci

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A AB BS ST TR RA AC CT T O Ob bj je ec ct ti iv ve e: : The purpose of the study was to investigate the effects of vitamin E in the protection of the lung from potential ischemia-reperfusion injury during elective coronary artery bypass graft surgery. M Ma at te er ri ia al l a an nd d M Me et th ho od ds s: : This controlled randomized single-center study included patients who underwent elective coronary bypass grafting (CABG) operation. Forty-nine patients were randomly divided into 2 groups. Water soluble Vitamin E (100 mg) in tepid saline (n=25) or tepid saline alone (n=24) was administered via the jugular vein before the aortic cross clamping. Serum total antioxidant capacity (TAC) levels and serum malonedialdehyde levels (MDA) were measured. Pulmonary biopsies were obtained before the aortic cross clamping and 60 minutes after removing the cross clamp. Biopsies were examined histopathologically under electron microscopy. R Re es su ul lt ts s: : Serum MDA levels at T1 (15 minutes after removal of the cross clamp) and T2 (30 minutes after removal of the cross clamp) were higher in the control group compared to the Vitamin group. Serum TAC levels at T1, T2 and T3 (60 minutes after removal of the cross clamp) were higher in the Vitamin E group compared to the control group. Histopathologic injury grade was lower in the Vitamin E group than in the control group. C Co on nc cl lu us si io on n: : Vitamin E was found to be protective against reperfusion induced oxidative injury in the early operative period.K Ke ey y W Wo or rd ds s: : Vitamin E; cardiopulmonary bypass; lung injury; reperfusion injury Ö ÖZ ZE ET T A Am ma aç ç: : Bu çalışmanın amacı, elektif koroner baypas cerrahisi sırasında, akciğerdeki potansiyel iskemi reperfüzyon hasarını önlemede E vitamininin etkinliğini değerlendirmektir. G Ge er re eç ç v ve e Y Yö ön nt te em ml le er r: : Bu kontrollü, randomize, tek merkezli çalışma, elektif koroner arter baypas greftleme (KABG) operasyonu geçiren hastalarda yapıldı. Çalışmaya toplam 49 hasta alındı ve hastalar rastgele 2 gruba ayrıldı. Yirmi beş olguya aortik kross klemp yerleştirilmeden önce suda eriyen 100 mg E vitamini içeren serum fizyolojik, 24 olguya ise sadece serum fizyolojik juguler ven yoluyla verildi. Serum total antioksidan kapasitesi (TAK) ve serum malondialdehit (MDA) düzeyleri ölçüldü. Aortic kross klemp yerleştirimeden önce ve kross klempin alınmasını takiben 60. dakikada akciğer biyopsisi alındı ve elektron mikroskopu altında histopatolojik olarak değerlendirildi. B Bu ul lg gu ul la ar r: : Serum MDA değerleri karşılaştırıldığında, T1 (kross klemp kaldırıldıktan 15 dakika sonra) ve T2 (kross klemp kaldırıldıktan 30 dakika sonra) değerleri kontrol grubunda, E vitamini grubunun değerlerine göre daha yüksek saptandı. Serum TAK değerleri karşılaştırıldığında, T1, T2 ve T3 (kross klemp kaldırıldıktan 60 dakika sonra) değerleri E vitamini grubunda, kontrol grubuna kıyasla daha yüksek saptandı. E vitamin grubunda histopatolojik hasarlanmanın, kontrol grubundakine göre daha az olduğu sapta...

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“…Through the above mechanism, one can hypothesize that free radicals and oxidants injure the vascular endothelium, which reduces NO production, which then leads to neutrophil infiltration. Furthermore, leukocyte activation fuels the release of large amounts of oxygen free radicals during and after CPB (2,9), which ultimately impair the availability of NO and alter the NO-receptor interactions, thus contributing to the mesenteric endothelial injury in our control group (positive feedback cycle). PARP inhibition, by interrupting this cycle, may reduce both neutrophil infiltration and free radical generation.…”

Section: Discussionmentioning

confidence: 99%

Poly(ADP-ribose) polymerase inhibitor PJ-34 reduces mesenteric vascular injury induced by experimental cardiopulmonary bypass with cardiac arrest

Andrási¹,

Blázovics²,

Szabó³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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-The aim of this study was to investigate effects of poly(ADP-ribose) polymerase (PARP) inhibition on mesenteric vascular function and metabolism in an experimental model of cardiopulmonary bypass (CPB) with cardiac arrest. Twelve anesthetized dogs underwent 90-min hypothermic CPB. After 60 min of cardiac arrest, reperfusion was started for 40 min following application of either saline vehicle (control, n ϭ 6) or a potent PARP inhibitor, PJ-34 (10 mg/kg iv bolus and 0.5 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 infusion for 20 min, n ϭ 6). PJ-34 led to better recovery of cardiac output (2.2 Ϯ 0.1 vs. 1.8 Ϯ 0.2 l/min in control) and mesenteric blood flow (175 Ϯ 38 vs. 83 Ϯ 4 ml/min, P Ͻ 0.05 vs. control) after reperfusion. The impaired vasodilator response of the superior mesenteric artery to acetylcholine, assessed in the control group after CPB (Ϫ32.8 Ϯ 3.3 vs. Ϫ57.6 Ϯ 6.6% at baseline, P Ͻ 0.05), was improved by PJ-34 (Ϫ50.3 Ϯ 3.6 vs. Ϫ54.3 Ϯ 4.1% at baseline, P Ͻ 0.05 vs. control). Although plasma nitrate/nitrite concentrations were not significantly different between groups, mesenteric nitric oxide synthase activity was increased in the PJ-34 group (P Ͻ 0.05). Moreover, the treated group showed a marked attenuation of mesenteric venous plasma myeloperoxidase levels after CPB compared with the control group (75 Ϯ 1 vs. 135 Ϯ 9 ng/ml, P Ͻ 0.05). Pharmacological PARP inhibition protects against development of post-CPB mesenteric vascular dysfunction by improving hemodynamics, restoring nitric oxide production, and reducing neutrophil adhesion. endothelial function; nitric oxide; neutrophil adhesion; hemodynamics THERE IS A LARGE BODY OF EVIDENCE suggesting that the mesenteric vasculature has to be considered a primary target in the development of gastrointestinal complications after surgical procedures involving cardiopulmonary bypass (CPB) and cardiac arrest (1,8,31,32). Indeed, CPB is known to induce a systemic inflammatory reaction with free radical release leading to endothelial dysfunction in the mesenteric micro-and macrocirculation (1, 31). Factors that are related to this damage include reduced expression and activity of the endothelial nitric oxide synthase (eNOS) and reduced L-arginine availability that results in reduced bioavailability of NO (2, 15). Moreover, increased production of superoxide leads to increased degradation of NO and the formation of oxidant peroxynitrite, a potent trigger of various forms of oxidative cell injury (4, 20).Current evidence suggests that an important candidate pathway of free radical-induced endothelial vascular injury involves the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1). PARP-1 inhibitors have been shown to diminish brain damage after cerebral ischemia (30), prevent myocardial injury in heart ischemia (28), and reduce renal ischemiareperfusion injury (18). In addition, several recent reports indicate that PARP inhibition counteracts the mesenteric dysfunction in ischemia-reperfusion (17), colon inflammation (35), and hemorrhagic (16) and endotoxemic shock (25).Because most ...

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Systemic pattern of free radical generation during coronary bypass surgery.

Cited by 57 publications

References 36 publications

Lipid Peroxidation and Cardiac Troponin T Release during Routine Cardiac Surgery

Lipid Peroxidation and Cardiac Troponin T Release during Routine Cardiac Surgery

The Efficacy of Vitamin E in the Prevention of Lung Ischemia-Reperfusion Injury After Cardiopulmonary Bypass in Open Heart Surgery

Poly(ADP-ribose) polymerase inhibitor PJ-34 reduces mesenteric vascular injury induced by experimental cardiopulmonary bypass with cardiac arrest

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